Evidence map›Paper›PMID 41299676›Full record

ReviewCell communication and signaling : CCS2025

ICOSL: more than a trigger of ICOS function.

Ian Stoppa, Alessia Provera, Sara Sacchetti, Nausicaa Clemente, Deepika Pantham, Foteini Christaki, Cristina Vecchio, Anteneh Nigussie Sheferaw, Roberta Rolla, Chiara Dianzani and 2 more

Abstract readReview
In one paragraph

Review in Cell communication and signaling : CCS, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

  1. Review
  2. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors.

Ian Stoppa *Department of Health Sciences and Interdisciplinary Research Center of Autoimmune Diseases (IRCAD), Università del Piemonte Orientale, Novara, 28100, Italy.
Alessia Provera *Department of Health Sciences and Interdisciplinary Research Center of Autoimmune Diseases (IRCAD), Università del Piemonte Orientale, Novara, 28100, Italy.
Sara SacchettiDepartment of Health Sciences and Interdisciplinary Research Center of Autoimmune Diseases (IRCAD), Università del Piemonte Orientale, Novara, 28100, Italy.
Nausicaa ClementeDepartment of Health Sciences and Interdisciplinary Research Center of Autoimmune Diseases (IRCAD), Università del Piemonte Orientale, Novara, 28100, Italy.
Deepika PanthamDepartment of Health Sciences and Interdisciplinary Research Center of Autoimmune Diseases (IRCAD), Università del Piemonte Orientale, Novara, 28100, Italy.
Foteini ChristakiDepartment of Health Sciences and Interdisciplinary Research Center of Autoimmune Diseases (IRCAD), Università del Piemonte Orientale, Novara, 28100, Italy.
Cristina VecchioDepartment of Health Sciences and Interdisciplinary Research Center of Autoimmune Diseases (IRCAD), Università del Piemonte Orientale, Novara, 28100, Italy.
Anteneh Nigussie SheferawDepartment of Health Sciences and Interdisciplinary Research Center of Autoimmune Diseases (IRCAD), Università del Piemonte Orientale, Novara, 28100, Italy.
Roberta RollaDepartment of Health Sciences and Interdisciplinary Research Center of Autoimmune Diseases (IRCAD), Università del Piemonte Orientale, Novara, 28100, Italy.
Chiara Dianzani *Department of Scienza e Tecnologia del Farmaco, University of Turin, Turin, 10124, Italy.
Salvatore Sutti *Department of Health Sciences and Interdisciplinary Research Center of Autoimmune Diseases (IRCAD), Università del Piemonte Orientale, Novara, 28100, Italy. salvatore.sutti@med.uniupo.it.
Umberto Dianzani *Department of Health Sciences and Interdisciplinary Research Center of Autoimmune Diseases (IRCAD), Università del Piemonte Orientale, Novara, 28100, Italy.

Funding

Fondazione AIRC per la ricerca sul cancro ETS IG 20714 and IG 27154
6 · The paper itself

Abstract

Inducible T-cell costimulator (ICOS) and its ligand ICOSL are members of the CD28 and B7 receptor families that play central roles in immune regulation. While the role of ICOS in T-cell activation and differentiation has been widely studied, increasing evidence indicates that ICOSL, which is broadly expressed across both immune and nonimmune cell types, also functions as a signaling receptor. This review focuses on ICOSL-mediated reverse signaling and its ability to modulate the behavior of ICOSL-expressing immune and stromal cells. In vitro, ICOSL activation induces cell type-specific responses, most notably regulating cell migration. In vivo, ICOSL signaling influences key processes such as tumor growth, bone remodeling, wound healing, liver regeneration, and sepsis. Taken together, these findings expand the conventional view of ICOSL as a passive ligand and suggest that ICOSL is a versatile immune modulator with therapeutic relevance in cancer, inflammatory, and fibrotic diseases.

Indexed as

Inducible T-Cell Co-Stimulator LigandInducible T-Cell Co-Stimulator ProteinAnimalsHumansSignal TransductionICOS protein, humanInducible T-Cell Co-Stimulator LigandInducible T-Cell Co-Stimulator ProteinAngiogenesisImmune checkpointsReverse signallingTumor microenvironment

Identifiers

PMID41299676
PMCPMC12750674

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.